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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The angiotensin I-converting enzyme (ACE) activity was studied in 2 experimental models of acute renal failure: (a) rats treated with a single injection of mercuric chloride (1.5 mg/kg) and (b) rats treated with a single injection of potassium dichromate (15 mg/kg). Rats were sacrificed 24 and 48 h after mercuric chloride or potassium dichromate injection. ACE activity was measured in urine, serum, and kidney. These data were compared with vehicle-treated rats. Rats with acute renal failure had proteinuria, polyuria, and decreased creatinine clearance. The damage to the kidney proximal tubule was evident by (a) the histological analysis at light and electron microscopy, (b) the augmentation in the urinary excretion of dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase, and (c) the low molecular weight proteinuria pattern. In addition, the histological analysis at the ultrastructural level showed normal glomeruli appearance. The above data suggest that the increased urinary excretion of enzymes and proteins in rats with acute renal failure is a consequence of tubular injury. Urinary and serum ACE activities increased and kidney ACE activity decreased. Our data suggest that the increase in urine ACE activity may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of injury to the proximal tubule.
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PMID:Urinary angiotensin I-converting enzyme activity is increased in experimental acute renal failure. 871 86

Experimental work from our laboratory has confirmed the protective power of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, the diabetic cataract too has been partially prevented. The protection slightly increased, when vanadium was administered in combination with vitamin E. This investigation has introduced a combination of Na3VO4 plus the lazaroid U-83836E, a liposoluble antioxidant much more efficacious than tocopherol, in order to improve the insufficient protection when vitamin E was used. Male Wistar rats, rendered diabetic with STZ, were treated for 12 weeks with Na3VO4 in drinking water, U-83836E carried by the food, or both. The most significant metabolic parameters (food and fluid intake, diuresis and excreted feces) were studied monthly by means of metabolic cages. Body weight, glycemia, glycosuria and proteinuria were also recorded. At week 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled. Circulation glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG) and fluorescent peroxides were evaluated at the end of the experiment. After the first month of treatment U-83836E improved significantly the protective effect of vanadate alone on polydipsia and polyuria, but more efficiently on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was observed also on HbA1c, NAG and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered per os, in a non invasive manner.
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PMID:[Protective effect on nephropathy and on cataract in the streptozotocin-diabetic rat of the vanadium-lazaroid combination]. 899 28

A six-month-old male Golden Retriever with a three-month history of polyuria and polydipsia was examined. Hematological examinations revealed nonregenerative anemia, azotemia, high serum creatinine level, hypercalcemia, hyperphosphatemia, hypercholesterolemia, hyperamylasemia, and low level of total serum protein. Urinalysis indicated mild proteinuria, and low specific gravity. Radiographic and ultrasonographic examinations revealed bilateral small sized kidneys. Histological examination by renal biopsy confirmed the diagnosis of renal dysplasia. Treatment with a dietary protein restriction, oral adsorbents, and dried aluminum hydroxide gel have been performed in this dog, and then, azotemia, high serum creatinine level, hypercalcemia, and hyperphosphatemia were improved. During 10 months after the initiation of treatments, no significant clinical change except polydipsia and polyuria has been observed.
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PMID:A control of a golden retriever with renal dysplasia. 936 46

Infantile cystinosis is a metabolic lysosomal storage disease of cystine affecting most of the body cells. The first symptoms appear after 5-6 months of life: anorexia, vomiting, polyuria, polydipsia and failure to thrive, associated with the signs of tubular Fanconi syndrome including glycosuria, proteinuria, loss of bicarbonate, phosphate, potassium, sodium, etc. Treatment with cysteamine is effective if started as early as possible. This treatment delays or prevents the spontaneous evolution toward end-stage renal failure, usually between 6 and 12 years of age, and also prevents growth stunting. In the long term, other organs may be involved like eye, thyroid, endocrine pancreas, muscle and central nervous system. The diagnosis is ascertained by leucocytes cystine assay, also useful for the follow up and the adjustment of the treatment. Prenatal diagnosis is available on chorionic sample. The gene of the disease is not yet identified but is known to map to chromosome 17.
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PMID:[Infantile cystinosis]. 936 13

A 29-year-old woman with a triplet pregnancy received emergency caesarean section in the 33rd week of pregnancy. She lost 2 babies, one of whom was a fetal death and the other a neonatal death. Three weeks before delivery, she was admitted to hospital suffering from vomiting, diarrhea and polyuria. There were no laboratory abnormalities such as a slightly elevated levels of liver enzymes, nor any clinical symptoms of preeclampsia. At the end of the operation, disseminated intravascular coagulation (DIC) occurred and HELLP syndrome was diagnosed. However, the hemoglobin level was in the normal range at this point. On the 2nd postoperative day, hemolytic anemia developed in spite of the resolution of other problems. We suggested that the hemolysis, which may have been caused by a latent hemoconcentration and a membrane disorder of the red cells, was an osmotic hemolysis. This case was unique for the following reasons; 1) a lack of symptoms of hypertension, proteinuria and edema, 2) complications due to diabetes insipidus, 3) postpartum severe hemolysis following latent hemoconcentration, and 4) slow progress of the condition after onset. Early detection of HELLP syndrome is difficult. It should be considered in the management of patients with unrecognizable hemoconcentration and nonspecific complications.
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PMID:[HELLP syndrome in triplet pregnancy complicated by DIC and transient diabetes insipidus]. 951 34

Post-reperfusion inflammation as well as anti-allograft response occur following kidney transplantation. We evaluated tissue damage by multiple renal indicators and searched for rejection predictors forewarning serum creatinine upturns. Twenty recipients (43 +/- 9 y; donors' age 35 +/- 16 y) of first renal grafts were studied. All through their hospital stay (35 +/- 18 d, range 17-75 d) we measured serum levels of urea, creatinine and electrolytes along with urinary excretion rates of total protein, albumin, enzymes (GGT, NAG, AAP) and electrolytes. During the period of observation, peaks were seen on the 1st day for serum creatinine, serum K+ and urine albumin output; on the 2nd day for urine Na+, GGT, AAP and protein excretion rates; on the 4th day for urea and creatinine outputs; on the 5th day for NAG output. On the 14th day, serum urea and creatinine as well as urine GGT, NAG, AAP, albumin and total protein were still elevated compared to 20 healthy control subjects. Delayed/slow graft function was observed in six recipients with higher pre-transplantation plasma lipids and lower donor HDL cholesterol. Hospital stay time was correlated with need for post-transplantation dialysis (p = 0.01) and recipient proteinuria by time 0 (TO) to day 3 (p = 0.02). Cold ischemia time was positively associated with 0-3 d serum creatinine, 0-3 d urinary urea and protein outputs (multiple r 0.9, p < 0.001). Multivariate analysis of longitudinal data showed that recipients' serum creatinine was positively correlated (p < 0.001) with urine AAP and negatively correlated with urine albumin, with diuresis volume and urine creatinine (p < 0.01). Serum creatinine elevations were preceded (previous 1-7 d) by increases in urinary indicators, the probability being higher in the presence of multiple simultaneous abnormalities. Useful parameters predictive of favorable graft outcome prior to transplantation included a brief cold ischemia time and a normal donor/recipient serum lipoprotein profile. Following transplantation, useful parameters were a high diuresis volume at time zero along with low urine NAG and high albumin outputs; early (first opst-graft 3 d) polyuria, low urea and GGT, high K, NAG and total protein excretions.
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PMID:Urinary excretion rates of multiple renal indicators after kidney transplantation: clinical significance for early graft outcome. 957 59

In the rat, a single subcutaneous injection of sodium dichromate (20 mg/kg) causes acute renal injury and significant polyuria, proteinuria, and glycosuria (peaking 2-3 days after treatment, and returning to normal by day 5) without any changes in the plasma levels of protein, glucose, and glycated haemoglobin. Surprisingly, the percentage levels of glycated plasma total proteins and albumin (assayed by boronate affinity chromatography) transiently and significantly decrease during recovery from proteinuria (days 4 and 10 after treatment) and were found in the normal range of values by day 18. These changes are concomitant with a significant increase in the percentage level of glycated albumin in urine. Constancy of total plasma protein and the temporal pattern of levels of glycation suggest that changes in the percentage values of glycated proteins are secondary to a transient selective loss of glycated plasma proteins in urine.
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PMID:Glycated plasma proteins in experimentally induced acute toxic renal failure by dichromate injection: evidence for loss with urine and decreased plasma levels. 974 56

Kidney is the main target organ of Cd toxicity in humans. Cd-induced nephrotoxicity is thought to be caused by the Cd-metallothionein complex (CdMT) that "leaks" out of the liver and is taken up by the kidney. A single injection of CdMT has therefore been used as a model to study Cd nephropathy for the last 20 years. However, our recent studies reveal discrepancies between renal Cd concentration and nephrotoxic potencies of CdCl2 and CdMT. This study was further designed to critically evaluate whether a single injection of CdMT is an appropriate model to study the mechanism of chronic CdCl2 nephropathy. Age-matched rats were given multiple sc injections of either CdCl2 (0.8 and 1.2 mg Cd/kg) or CdMT (0.05 mg Cd/kg) daily, 6 days/week for 6 weeks, or a single injection of CdMT (0.2-0.6 mg Cd/kg i.p. for 24 h), and the nephrotoxicity was compared. Histologically, chronic CdCl2 or CdMT administration produced damage to the whole kidney, including tubular cell degeneration, apoptosis, and atrophy; interstitial inflammation; glomerular swelling; and sclerosis. In contrast, acute CdMT injection produced severe proximal tubule necrosis as the major feature of its toxicity. Biochemically, chronic exposure to Cd produced polyuria and calciuria, while proteinuria, glucosuria, and enzymuria were mild (2-5x). In contrast, acute CdMT nephrotoxicity was characterized by marked increases in urinary protein (13x), glucose (25x), N-acetyl-beta-d-glucosaminidase (28x), lactate dehydrogenase (100x), and gamma-glutamyltranspeptidase (160x). Serum levels of creatinine and blood urea nitrogen were unchanged following chronic Cd exposure but were markedly elevated (5x) after acute injection of CdMT. Chronic exposure to either CdCl2 or CdMT produced nephrotoxicity at renal Cd concentration of 85 to 110 micrograms/g kidney, while acute CdMT injection produced nephrotoxicity at only 5 to 7 micrograms/g kidney. In conclusion, the present study indicates that the features and mechanisms of renal injury from chronic Cd exposure are quite different from those produced by a single injection of CdMT. Therefore, it is proposed that acute CdMT injection is not an appropriate model for the study of chronic Cd-induced nephrotoxicity.
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PMID:Acute CdMT injection is not a good model to study chronic Cd nephropathy: comparison of chronic CdCl2 and CdMT exposure with acute CdMT injection in rats. 987 99

A six-month-old Labrador retriever was presented for investigation of acute polyuria, polydipsia and haematemesis six hours following ingestion of a tube of the topical antipsoriatic vitamin D analogue, calcipotriol. Transient hypercalcaemia, azotaemia, proteinuria, thrombocytopenia and ventricular arrhythmias ensued. Abdominal ultrasonography and echocardiography revealed evidence of diffuse soft tissue mineralisation. Despite 13 days of intensive supportive care, the dog was euthanased due to continued haematemesis and anorexia. Necropsy confirmed mineralisation and necrosis of multiple organ systems consistent with vitamin D toxicity.
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PMID:Calcipotriol toxicity in a dog. 1064 1

We encountered a patient with megaureter-megacystis syndrome showing a giant bladder and dilated ureters with marked reflux, which is very rare; to our knowledge, only 2 patients have been reported in Japan. The patient was a 4-year-old boy, who showed inborn polyposia and polyuria, and proteinuria at the age of 1 year. He visited the pediatric department in our hospital complaining of cold-like symptoms, stomachache and diarrhea. Urinary infection and kidney dysfunction were observed, and the patient was hospitalized for close examination. Bilateral pyelocaliceal hydronephrosis was detected by ultrasonography, and the patient was referred to our department. CT revealed bilateral hydronephrosis (right atrophic kidney), hydroureters and megacystis. Bilateral grade V vesicoureteral reflux, an increase in the bladder volume (> 300 ml), and urination without residual urine were noted by voiding cystourethrography. Uroflowmetry revealed that maximum flow rate was 21.6 ml/sec, voided volume was 110 ml, and residual volume was 24 ml. From these examinations, the patient was diagnosed as having megaureter-megacystis syndrome, and underwent antireflux operation of the bilateral ureters using Cohen's procedures.
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PMID:[The so-called megaureter-megacystis syndrome: a case report]. 1051 89


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